Heart failure is a debilitating disease in which abnormal function of the heart leads to inadequate blood flow to fulfill the needs of the tissues and organs of the body. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately fill with blood between heartbeats and the valves regulating blood flow become leaky, allowing regurgitation or back-flow of blood. The impairment of arterial circulation may deprive vital organs of oxygen and nutrients. Fatigue, weakness and the inability to carry out daily tasks may result. Not all heart failure patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive.
As heart failure progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds cardiac muscle mass causing the ventricles to grow in volume in an attempt to pump more blood with each heartbeat, i.e. to increase the stroke volume. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result, typically in the form of myocardial ischemia or myocardial infarction. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output. Often, electrical and mechanical dyssynchronies develop within the heart such that the various chambers of the heart no longer beat in a synchronized manner, degrading overall cardiac function. A particularly severe form of heart failure is congestive heart failure (CHF) wherein the weak pumping of the heart or compromised filling leads to build-up of fluids in the lungs and other organs and tissues.
Pulmonary edema (PE) is a swelling and/or fluid accumulation in the lungs often caused by heart failure. Briefly, the poor cardiac function resulting from heart failure can cause blood to back up in the lungs, thereby increasing blood pressure in the lungs, particularly pulmonary venous pressure. The increased pressure pushes fluid—but not blood cells—out of the blood vessels and into lung tissue and air sacs (i.e. the alveoli). This can cause severe respiratory problems and, left untreated, can be fatal. PE can also arise due to other factors besides heart failure, such as infections.
In view of the potential severity of CHF/PE, it is highly desirable to detect the conditions so that appropriate therapy can be provided. Many patients susceptible to CHF and PE are candidates for pacemakers, ICDs, cardiac resynchronization therapy (CRT) devices or sub-Q monitors such as implantable loop recorders (ILRs). Accordingly, it would be helpful to provide techniques for detecting and tracking CHF and/or PE using such implantable devices.
One useful parameter for detecting and tracking CHF/PE is LAP, i.e. the blood pressure within the left atrium of the patient. Reliable detection or estimation of LAP would permit the implanted device to track fluid overloads associated with CHF/PE for diagnostic purposes and to also control therapies such as the administration of diuretics in response to PE or the delivery of CRT in response to heart failure.
However, LAP is a difficult parameter to detect since it is not clinically appealing to place a blood pressure sensor directly in the left atrium due to the chronic risk of thromboembolic events, as well as risks associated with the trans-septal implant procedure itself. Accordingly, various techniques have been developed for estimating LAP based on other parameters that can be more safely sensed by an implantable medical device. In particular, a number of techniques have been developed that use electrical impedance (Z) to estimate LAP. For example, intracardiac impedance can be sensed along a sensing vector passing through the left atrium, such as between an electrode mounted on a left ventricular (LV) lead and another electrode mounted on a right atrial (RA) lead. The impedance is affected by the blood volume inside the left atrium, which is in turn reflected by the pressure in the left atrium. Accordingly, there is a correlation between the detected impedance and LAP, which can be exploited to estimate LAP and also track CHF and fluid overloads associated with PE.
Techniques for exploiting impedance measurements to estimate LAP are referred to herein as zLAP estimation techniques. See, for example, U.S. Provisional Patent Application No. 60/787,884 of Wong et al., entitled, “Tissue Characterization Using Intracardiac Impedances with an Implantable Lead System,” filed Mar. 31, 2006, and U.S. patent application Ser. Nos. 11/558,101; 11/557,851; 11/557,870; 11/557,882; and 11/558,088, each entitled “Systems and Methods to Monitor and Treat Heart Failure Conditions,” of Panescu et al. See, also, U.S. patent application Ser. No. 11/558,194, by Panescu et al., entitled “Closed-Loop Adaptive Adjustment of Pacing Therapy based on Cardiogenic Impedance Signals Detected by an Implantable Medical Device.”
Particularly effective techniques for calibrating zLAP estimation techniques are set forth in: U.S. patent application Ser. No. 11/559,235, by Panescu et al., entitled “System and Method for Estimating Cardiac Pressure Using Parameters Derived from Impedance Signals Detected by an Implantable Medical Device” and U.S. patent application Ser. No. 12/109,304, filed Apr. 25, 2008, of Gutfinger et al., entitled “System and Method for Calibrating Cardiac Pressure Measurements derived from Signals Detected by an Implantable Medical Device.”
Although early zLAP preclinical data has demonstrated promising results, impedance-based estimates of LAP are still susceptible to non-cardiogenic influences on impedance, such as pneumonia. Accordingly, it would be desirable to develop LAP detection techniques that do not rely exclusively on impedance but additionally or alternatively exploit other parameters detectable by implantable devices to assess LAP. It is to this end that various aspects of the present invention are directed.
Rather than estimating LAP based on zLAP, techniques have been developed that estimate LAP based on conduction delays measured within electrocardiac signals. See, U.S. patent application Ser. Nos. 11/779,350 and 11/779,380, of Wenzel et al., filed Jul. 18, 2007, and both entitled “System and Method for Estimating Cardiac Pressure based on Cardiac Electrical Conduction delays using an Implantable Medical Device.” Techniques are described therein for estimating LAP or other cardiac performance parameters based on measured interventricular (RV-LV) conduction delays or atrioventricular (AV) conduction delays. Predetermined conversion factors stored within the device are used to convert measured conduction delays into LAP values.
It would be desirable to develop techniques that exploit still other electrocardiac intervals or other electrocardiac morphological parameters to detect LAP, and it is to this end that various other aspects of the present invention are directed.